Emma Holliday for Surgery: Part II Flashcards
Clotting in old people? Think:
Cancer
Clotting with edema, HTN and foamy pee?
Nephrotic Syndrome
Clotting in a young person with a positive family history for clotting?
Factor V Leiden
Why do we care about AT III deficiency?
Heparin won’t work
When we have a young woman with multiple SABs (spontaneous abortions) what do we think is happening?
Lupus Anticoagulant
In post op patients with low platelets and clots, what most likely occurred?
HIT - Heparin induced thrombocytopenia if Heparin was given 5- 14 days post-op.
Further information: There are two types of HIT. Type 1 HIT presents within the first 2 days after exposure to heparin, and the platelet count normalizes with continued heparin therapy. Type 1 HIT is a nonimmune disorder that results from the direct effect of heparin on platelet activation. Type 2 HIT is an immune-mediated disorder that typically occurs 4-10 days after exposure to heparin and has life- and limb-threatening thrombotic complications. In general medical practice, the term HIT refers to type 2 HIT
How do we treat post-op patients with HIT?
Leparudin or agatroban
If I have bleeding with isolated decrease in platelets, what is occurring?
ITP
Further information: Immune thrombocytopenic purpura (ITP) is a clinical syndrome in which a decreased number of circulating platelets (thrombocytopenia) (see the image below) manifests as a bleeding tendency, easy bruising (purpura), or extravasation of blood from capillaries into skin and mucous membranes (petechiae). Although most cases of acute ITP, particularly in children, are mild and self-limited, intracranial hemorrhage may occur when the platelet count drops below 10 × 109/L (
If I am bleeding, have normal platelets, but an increased bleeding time and PTT, what do we have going on?
vWD
Further information: Von Willebrand disease (vWD) is a common, inherited, genetically and clinically heterogeneous hemorrhagic disorder caused by a deficiency or dysfunction of the protein termed von Willebrand factor (vWF). Consequently, defective vWF interaction between platelets and the vessel wall impairs primary hemostasis.
vWF, a large, multimeric glycoprotein, circulates in blood plasma at concentrations of approximately 10 mg/mL. In response to numerous stimuli, vWF is released from storage granules in platelets and endothelial cells. It performs two major roles in hemostasis. First, it mediates the adhesion of platelets to sites of vascular injury. Second, it binds and stabilizes the procoagulant protein factor VIII (FVIII)
What does DIC look like?
- low platelets
- low fibrinogen
- high PT
- high PTT
- high BT (bleeding time)
- high d-dimer
- Schistocytes
What causes DIC?
Gram negative sepsis, carcinomatosis, OB stuff
Rule of 9s for burns
You can review this.
Parkland formula
The Parkland formula is a burn formula used to estimate the amount of replacement fluid required for the first 24 hours in a burn patient so as to ensure they remain hemodynamically stable
Resuscitation fluids: 3-4 mL Ringer lactate or normal saline (2 - 4 in kiddos) X weight (kg) X %TBSA burned (second-degree and third degree); half administered over the first 8 hours (from time of injury), remaining half administered over the next 16 hours
For burn patients, we can’t give them PO or IV antibiotics (communication to the skin from inside is compromised). So we give topical antibiotics to these patients.
Which topical agent doesn’t penetrate an eschar and can cause leukopenia?
Silver Sulfadiazine
For burn patients, we can’t give them PO or IV antibiotics (communication to the skin from inside is compromised). So we give topical antibiotics to these patients.
Which topical agent penetrates the eschar, but hurts like hell?
Mafenide
For burn patients, we can’t give them PO or IV antibiotics (communication to the skin from inside is compromised). So we give topical antibiotics to these patients.
Which topical agent doesn’t penetrate an eschar and can cause hypokalemia and hyponatremia?
Silver nitrate
What can we do prior to leaving for the ED when we have a chemical burn?
Irrigate for more than 30 min
What’s the best first step in an electrical burn?
EKG
In an electrical burn, if our EKG is abnormal, what is our next step?
48 hours of Telemetry (also if LOC with normal EKG)
If the urine dipstick is positive for blood but microscopic exam is negative for RBCs, what is going on?
It means we have myoglobinuria due to ATN.
If we find myoglobinuria, what do we next do?
Check their K+ levels. We need potassium for our muscles to contract. Low potassium means less contracting which means muscle wasting and breakdown. This increases products like myoglobin in the blood which can damage kidneys. We see myoglobin in the urine, with the worst form being rhabdomyolysis.
Describe compartment syndrome
Often seen with a burn injury to an extremity, making it extremely tender, numb, white, cold, and barely papable pulses.
One of two criteria fulfilled:
- 5P’s - Pain, pulse, parasthesia, palor, paralysis
- Compartment pressure > 30mmHg
Is compartment syndrome linked to hypokalemia?
Compartment syndrome is a self-perpetuating cascade of events. It begins with the tissue edema that normally occurs after injury (eg, because of soft-tissue swelling or a hematoma). If edema develops within a closed fascial compartment, typically in the anterior or posterior compartments of the leg, there is little room for tissue expansion, so interstitial (compartment pressure) increases. As compartmental pressure exceeds the normal capillary pressure of about 8 mm Hg, cellular perfusion slows and may ultimately stop. (NOTE: Because 8 mm Hg is much lower than arterial pressure, cellular perfusion can stop long before pulses disappear.) Resultant tissue ischemia further worsens edema in a vicious circle.
As ischemia progresses, muscles necrose, sometimes leading to rhabdomyolysis, infections, and hyperkalemia; these complications can cause loss of limb and, if untreated, death. Hypotension or arterial insufficiency can compromise tissue perfusion with even mildly elevated compartment pressures, causing or worsening compartment syndrome.
